Hi I'm Abhinav, I'm 15 years old and I am from Wilmington, Delaware. I am a rising 10th grader at my local public school, Concord High School. I am especially interested in math and science. I want to going into a career in engineering but I don't know what type of engineering yet. That's why I'm here; I want to explore different fields in math and science before I decided what I would like to pursue. I am interested in computer science especially, but I have yet to take a biology course and so I thought this would be an opportunity to extend my scientific knowledge. My other interests including playing the piano as well as playing sports, especially soccer and tennis. I like many different types of music, especially rap and hip-hop music. I also like to travel and have been to India to visit family and visit landmarks such as the Taj Mahal. I have also been to Germany as a part of an exchange program at my school. I went to one of the most famous landmarks in Germany, the Bastei Bridge. I hope to learn a lot from this camp and I am very excited.
My Project: Escherischia Coli O157:H7 and Antibiotics
Escherischia Coli is one the most thoroughly studied bacteria in the world. We know that most E. Coli bacteria are harmless to humans and in some cases necessary for humans to function properly. E. Coli bacteria have numerous benefits including easier digestion, increase immune response, and decreased intestinal problems. However, out of the many, many different types of E. Coli bacteria there are some that are pathogenic and harmful to humans. Pathogenic E. Coli are differentiated into 6 pathotypes. A majority of E. Coli infections are as a result of Shiga-toxin producing E. coli (STEC). They are also known as Verocytotoxin-producing E. coli (VTEC) or enterohemorrhagic E. coli (EHEC). Within the STEC pathotype, most cases are identified as E. Coli O157:H7 infections. In this instance, O depicts the marker on the surface of the bacteria and the H refers to the markers on the flagellum of the bacteria. While these markers have nothing to do with the pathogenicity or lethality of the bacterium, they help scientists to identify which strain of E. Coli they are working with.
E. Coli was discovered in 1885 by Theodore von Escherisch. It has been studied extensively in the last 130 years and they have been discovered to be for the most part a helpful bacteria. Most E. Coli bacteria are located in the intestines of healthy human beings and help in digestion. However, E. Coli O157:H7, also known as E. Coli O157 or just O157, was first identified as a pathogen in 1982. Multiple outbreaks have occurred since its identification. These have been caused by many different foods and beverages including drinking water, apple cider and even hamburgers. In 1985, O157 was determined to be a cause of HUS, hemolytic uremic syndrome. Many outbreaks have occurred since then, the largest of which was caused by undercooked beef. In 1993, a company called Jack in the Box started selling undercooked hamburger patties in many different restaurants all over the country. Over 700 people were infected making it the biggest foodborne outbreak in American history. A majority of the victims were children, and four children died. In addition, over 175 people suffered from permanent kidney damage as a result HUS. To this day, O157 continues to cause sickness throughout America causing over 100,000 cases and 3,200 hospitalizations each year.
E. Coli O157:H7 can cause bloody diarrhea, abdominal cramps and has also been linked to an increased risk of HUS. HUS can lead to kidney failure and other complications. The sequence of events from diarrhea to kidney failure is all caused by the Shiga toxin that is produced by these particular E. Coli bacteria. As the bacteria multiply within the large intestine, they attach themselves to the walls of the intestine and this bond allows them to start producing the Shiga toxin. This toxin attached to white blood cells which travel to the kidneys where it attaches to its receptor glycolipid globotriaosylceramide, abbreviated as Gb3. These receptors are also located in other parts of the body so patients may develop complications in other organs. This toxin causes injury and even death to cells causing blood to clot and lead the kidney to fail. As the blood vessels become partially obstructed, red blood cells are killed either directly by the toxin, or they are damaged as they attempt to pass through the obstructed vessels. As stated before, the Shiga toxin can be very harmful to humans and its main source is the STEC pathotype of E. Coli. Shiga belongs to the AB5 class of toxins. The AB5 class consists of six-component protein complexes, which are vital to the virulence of many different bacterial infections. These complexes are the key agents in many illnesses including whooping cough, cholera, and of course hemorrhagic diarrhea and HUS. Outbreaks of diseases caused by these toxins have claimed thousands of lives making them some of the most dangerous class of toxins in the world. Shiga toxins especially have been at the center of over 40 outbreaks in the US alone since 1999 and kills about 500 people each year in America. In all of these toxins, the A subunit is responsible for causing harm to the cells and the B subunit is responsible for finding and bonding to the host cells within the body. The A part is divided into two sections labeled A1 and A2. These two sections are connected by a disulfide bond. A1 contains all the information to be toxic to the host cells and is responsible for the actual cell injury. Stx1 and Stx2, the types of Shiga toxin produced by STEC, remove a certain adenine base from the cells’ RNA, rendering it unable to carry out protein synthesis which in turn causes the cell to die. The A2 domain anchors the entire A subunit to the B subunit without using covalent bonds. The B subunit is responsible for recognizing and binding to the receptors of the surface of host cells. In Shiga toxins, the oligosaccharide and oligonucleotide folds are present, which is common to most of the pathogens in the AB5. Stx1 and most of the Stx2 varieties bond to the oligosaccharide component of Gb3, but Stx2e binds to Gb4. In our body, Gb3 is located specifically on the surface of the kidneys which is why ingestion of E. Coli O157:H7 can cause HUS.
In most E. Coli infections, the patient will heal within five to ten days. However, if the patient develops further complications such as HUS, further steps need to be made. Antibiotics are an option that doctors avoid in this situation because they can increase the chance that the patient will develop more serious symptoms. However, for seven percent the patients that do develop complications such as HUS, dialysis is necessary. Unfortunately, there is no good treatment for HUS and it claims many lives each year.
In order to prevent the O157 bacteria from producing the Shiga toxin which is so harmful to humans, scientists have studied what causes the bacteria to produce this toxin. They have found that it is SOS reaction which is caused by damage to the bacteria’s DNA. When this DNA is damaged, the SOS genes are activated and the repression of certain genes is broken down. This happens because when the cell is damaged, it interacts with the RecA protein. This protein has many functions, but it also causes the LexA protein and the Cl protein to degrade. This two proteins are instrumental in repressing the genes within the cell that produce Stx1 and Stx2. This is why antibiotics often lead to more complications in patients with E. Coli, the medicines attack the bacteria causing it to produce more and more Shiga toxin. In order to stop the bacteria from producing this toxin, they must either not be attacked, or their response to damaged DNA must be altered. The RecA protein is only activated when there is a break in the cell’s DNA. If the gene that produces this protein, known as the recA gene, was removed in E. Coli O157 bacteria, when the antibiotics attacked it, it would still trigger an SOS response, but the RecA protein would not be produced. This would mean that the LexA and Cl proteins would still be active and the cell would not regrow. This would disable the bacteria’s ability to produce the Shiga toxin which would render it harmless to humans. Additionally, antibiotics could be used to kill these bacteria without the worry of inadvertently releasing toxins. The E. Coli O157:H7 bacteria is a very harmful bacteria that can causes hemorrhagic diarrhea, vomiting, HUS and even brain damage. This bacteria, without any modifications, cannot be treated with antibiotics because damage caused to the cell would cause it to create more Shiga toxin.
My Project: Escherischia Coli O157:H7 and Antibiotics
Escherischia Coli is one the most thoroughly studied bacteria in the world. We know that most E. Coli bacteria are harmless to humans and in some cases necessary for humans to function properly. E. Coli bacteria have numerous benefits including easier digestion, increase immune response, and decreased intestinal problems. However, out of the many, many different types of E. Coli bacteria there are some that are pathogenic and harmful to humans. Pathogenic E. Coli are differentiated into 6 pathotypes. A majority of E. Coli infections are as a result of Shiga-toxin producing E. coli (STEC). They are also known as Verocytotoxin-producing E. coli (VTEC) or enterohemorrhagic E. coli (EHEC). Within the STEC pathotype, most cases are identified as E. Coli O157:H7 infections. In this instance, O depicts the marker on the surface of the bacteria and the H refers to the markers on the flagellum of the bacteria. While these markers have nothing to do with the pathogenicity or lethality of the bacterium, they help scientists to identify which strain of E. Coli they are working with.
E. Coli was discovered in 1885 by Theodore von Escherisch. It has been studied extensively in the last 130 years and they have been discovered to be for the most part a helpful bacteria. Most E. Coli bacteria are located in the intestines of healthy human beings and help in digestion. However, E. Coli O157:H7, also known as E. Coli O157 or just O157, was first identified as a pathogen in 1982. Multiple outbreaks have occurred since its identification. These have been caused by many different foods and beverages including drinking water, apple cider and even hamburgers. In 1985, O157 was determined to be a cause of HUS, hemolytic uremic syndrome. Many outbreaks have occurred since then, the largest of which was caused by undercooked beef. In 1993, a company called Jack in the Box started selling undercooked hamburger patties in many different restaurants all over the country. Over 700 people were infected making it the biggest foodborne outbreak in American history. A majority of the victims were children, and four children died. In addition, over 175 people suffered from permanent kidney damage as a result HUS. To this day, O157 continues to cause sickness throughout America causing over 100,000 cases and 3,200 hospitalizations each year.
E. Coli O157:H7 can cause bloody diarrhea, abdominal cramps and has also been linked to an increased risk of HUS. HUS can lead to kidney failure and other complications. The sequence of events from diarrhea to kidney failure is all caused by the Shiga toxin that is produced by these particular E. Coli bacteria. As the bacteria multiply within the large intestine, they attach themselves to the walls of the intestine and this bond allows them to start producing the Shiga toxin. This toxin attached to white blood cells which travel to the kidneys where it attaches to its receptor glycolipid globotriaosylceramide, abbreviated as Gb3. These receptors are also located in other parts of the body so patients may develop complications in other organs. This toxin causes injury and even death to cells causing blood to clot and lead the kidney to fail. As the blood vessels become partially obstructed, red blood cells are killed either directly by the toxin, or they are damaged as they attempt to pass through the obstructed vessels.
As stated before, the Shiga toxin can be very harmful to humans and its main source is the STEC pathotype of E. Coli. Shiga belongs to the AB5 class of toxins. The AB5 class consists of six-component protein complexes, which are vital to the virulence of many different bacterial infections. These complexes are the key agents in many illnesses including whooping cough, cholera, and of course hemorrhagic diarrhea and HUS. Outbreaks of diseases caused by these toxins have claimed thousands of lives making them some of the most dangerous class of toxins in the world. Shiga toxins especially have been at the center of over 40 outbreaks in the US alone since 1999 and kills about 500 people each year in America. In all of these toxins, the A subunit is responsible for causing harm to the cells and the B subunit is responsible for finding and bonding to the host cells within the body. The A part is divided into two sections labeled A1 and A2. These two sections are connected by a disulfide bond. A1 contains all the information to be toxic to the host cells and is responsible for the actual cell injury. Stx1 and Stx2, the types of Shiga toxin produced by STEC, remove a certain adenine base from the cells’ RNA, rendering it unable to carry out protein synthesis which in turn causes the cell to die. The A2 domain anchors the entire A subunit to the B subunit without using covalent bonds. The B subunit is responsible for recognizing and binding to the receptors of the surface of host cells. In Shiga toxins, the oligosaccharide and oligonucleotide folds are present, which is common to most of the pathogens in the AB5. Stx1 and most of the Stx2 varieties bond to the oligosaccharide component of Gb3, but Stx2e binds to Gb4. In our body, Gb3 is located specifically on the surface of the kidneys which is why ingestion of E. Coli O157:H7 can cause HUS.
In most E. Coli infections, the patient will heal within five to ten days. However, if the patient develops further complications such as HUS, further steps need to be made. Antibiotics are an option that doctors avoid in this situation because they can increase the chance that the patient will develop more serious symptoms. However, for seven percent the patients that do develop complications such as HUS, dialysis is necessary. Unfortunately, there is no good treatment for HUS and it claims many lives each year.
In order to prevent the O157 bacteria from producing the Shiga toxin which is so harmful to humans, scientists have studied what causes the bacteria to produce this toxin. They have found that it is SOS reaction which is caused by damage to the bacteria’s DNA. When this DNA is damaged, the SOS genes are activated and the repression of certain genes is broken down. This happens because when the cell is damaged, it interacts with the RecA protein. This protein has many functions, but it also causes the LexA protein and the Cl protein to degrade. This two proteins are instrumental in repressing the genes within the cell that produce Stx1 and Stx2. This is why antibiotics often lead to more complications in patients with E. Coli, the medicines attack the bacteria causing it to produce more and more Shiga toxin. In order to stop the bacteria from producing this toxin, they must either not be attacked, or their response to damaged DNA must be altered.
The RecA protein is only activated when there is a break in the cell’s DNA. If the gene that produces this protein, known as the recA gene, was removed in E. Coli O157 bacteria, when the antibiotics attacked it, it would still trigger an SOS response, but the RecA protein would not be produced. This would mean that the LexA and Cl proteins would still be active and the cell would not regrow. This would disable the bacteria’s ability to produce the Shiga toxin which would render it harmless to humans. Additionally, antibiotics could be used to kill these bacteria without the worry of inadvertently releasing toxins.
The E. Coli O157:H7 bacteria is a very harmful bacteria that can causes hemorrhagic diarrhea, vomiting, HUS and even brain damage. This bacteria, without any modifications, cannot be treated with antibiotics because damage caused to the cell would cause it to create more Shiga toxin.